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Biomedical subjects

M L Sears

Publications and source records attributed to M L Sears.

At least 55 records · Page 3Linked to original sources

Objective evaluation of experimental ocular irritation.

After topically administered nitrogen mustard the irritative effect on the pupil, intraocular pressure, protein concentration of the aqueous humor and on the vessels of the iris and conjunctiva was quantified. The protein level in aqueous was determined by refractometry. The degree of hyperemia of conjunctiva and iris was determined by measuring the amount of Evans blue dye present in the tissue minutes after intravenous administration. A reproducible relationship was obtained using these methods to evaluate the degree of irritation produced by nitrogen mustard.

Animals↗

The effect of dopamine on the intraocular pressure and pupil of the rabbit eye.

The presence of a dopamine-specific receptor that can influence intraocular pressure in the rabbit eye is suggested by these experiments: intravitreal, systemic, or topically administered dopamine solutions can produce a decrease in intraocular pressure that is dose-dependent. In high doses the decrease in intraocular pressure is accompanied by mydriasis, and alpha-adrenergic pupillary response. This alpha-response may be caused by dopamine as a direct, but weak alpha-stimulator or by displacement of norepinephrine onto the receptor from its storage site. At lower doses the decrease in intraocular pressure occurs in the absence of mydriasis and in spite of blockade of beta-adrenergic receptors. Further, a specific dopaminergic blocker, haloperidol, prevents this decrease in intraocular pressure. The decreases are small, but reproducible and suggest that dopamine can influence the adrenergic regulation of intraocular pressure.

Administration, Topical↗

The effect of d-isoproterenol on intraocular pressure of the rabbit, monkey, and man.

D-isoproterenol d-bitartrate applied topically lowers intraocular pressure (IOP) in normal albino rabbits and rabbits with alpha-chymotrypsin-induced glaucoma. This effect is independent of any effect on systemic blood pressure or pulse rate. A similar response could not be obtained in monkey or human eyes. Subconjunctival injection of d-isoproterenol d-bitartrate to monkey eyes did not alter IOP.

Administration, Topical↗

The contralateral effect of antidromic stimulation of the trigeminal nerve on the rabbit eye.

The effect on contralateral eyes after injuries to one eye has been called the consensual reaction and has been postulated to be either the consequence of a neural reflex or one achieved by circulating substances. Trigeminal stimulation always causes ipsilateral miosis, ocular hyperemia, intraocular hypertension, and a disruption of the blood-aqueous barrier. Disruption of the blood-aqueous barrier in the contralateral eye after stimulation of the trigeminal nerve always occurs and depends on intact sensory innervation to that globe in rabbits. The disruption is not prevneted by pretreatment of the animals with indomethacin. The phenomenon of disruption of the barrier is sometimes accompanied by an elevation of intraocular pressure in the contralateral eye but not by the other irritative responses. Thus, unilateral stimulation of a sensory nerve, the trigeminal, in the rabbit, can produce ipsilateral contralateral disruption of the blood-aqueous barrier.

Animals↗

Potentiation of the effects of topical epinephrine on the pupil and intraocular pressure in the sympathetically denervated rabbit eye by a catechol-O-methyl transferase inhibitor.

Dose-response curves of increase in pupil size and decrease in intraocular pressure with topical epinephrine have been determined in the sympathetically denervated rabbit eye. Topical pretreatment with the catechol-O-methyl transferase inhibitor U-0521 potentiated the effects of epinephrine on both the pupil and pressure. These observations suggest a possible role for catechol-O-methyl transferase in the aqueous humor dynamics of the supersensitive eye. The possible use of the denervated rabbit eye as an experimental model for the glaucomatous eye in evaluating the ocular effects of adrenergic agents is discussed.

Administration, Topical↗

Morphology of the breakdown of the blood-aqueous barrier in the ciliary processes of the rabbit eye after prostaglandin E2.

Protaglandin E2, administered topically to the rabbit eye, causes disruption of the blood-aqueous barrier resulting in a large increase in the protein content of the aqueous humor. The route of plasma proteins into the aqueous humor was studied with the electron microscope, using horseradish peroxidase as a protein tracer. The tracer penetrated the tight junctions of the nonpigmented layer of the ciliary epithelium, filling the lateral intercellular clefts and staining the internal limiting membrane. These morphological studies confirm the prior physiologic demonstration that, in response to prostaglandin, plasma proteins enter the posterior chamber via the intercellular clefts of the nonpigmented epithelium.

Administration, Topical↗

Pathways for the response of the eye to injury.

The role of a neural pathway in the disruption of the blood-aqueous barrier of the rabbit after two irritating stimuli, topical nitrogen mustard, and paracentesis, was studied. Retrobulbar anesthesia or section of the ophthalmic division of the trigeminal nerve decreased the breakdown of the blood-aqueous barrier, as measured by protein in the aqueous humor, after topical nitrogen mustard. Sensory denervation, accomplished with retrobulbar alcohol, virtually prevented the protein rise in the aqueous humor. Disruption of the blood-aqueous barrier after paracentesis, however, was not affected by retrobulbar anesthesia or alcohol denervation. Therefore, the increased protein in the aqueous humor after an irritative stimulus appears to be mediated by at least two pathways. The response to a stimulus such as nitrogen mustard depends on sensory innervation and is not mediated by prostaglandins to any important degree. The response to paracentesis does not require sensory innervation and appears to be mediated, at least in part, by prostaglandins.

Animals↗

Adenosine 3',5'-monophosphate increases the outflow of aqueous humor from the rabbit eye.

Direct administration of cyclic-AMP into the anterior chamber increases the outflow facility of the eye for aqueous humor. This is consistent with the hypothesis that catecholamines lower the intraocular pressure of the rabbit eye, at least in part, by a cyclic-AMP-mediated mechanism. This mechanism is active in the outflow channels and increases the rate at which aqueous humor leaves the anterior chamber.

Animals↗

Adenosine 3',5'-monophosphate analogue increases the outflow facility of the primate eye.

Our previous studies showed that cyclic-AMP increases the outflow facility of the eye of the rabbit. In this investigation, an analogue of cyclic-AMP, the 8-methylthio derivative, perfused into the anterior chamber of the eye of the vervet monkey, increased outflow facility twofold. This observation supports the hypothesis that cyclic-AMP mediates the action of adrenergic agents to reduce intraocular pressure in the primate eye.

Animals↗